Search

Relationships between avian physiology and bacterial assemblages in the cloaca are poorly understood. We used molecular techniques to analyze cloacal swabs from pigeons that were subjected to two immunological manipulations: lysozyme supplementation and endotoxin challenge. From the swabs, we derived ecological indices of evenness, richness, and diversity of bacterial assemblages. Challenge led to changes in evenness that depended on supplementation. When analyzing these changes, we neutralized the effects of a possible statistical artifact by including the starting values as a covariate. Repeatability calculations suggested that swabbing reliably captured the evenness but not the richness or diversity of bacterial assemblages in the cloaca.

Echocardiographic measurements were obtained before and 4 and 7 h after intraperitoneal challenge with endotoxin (Escherichia coli 0111:B4 lipopolysaccaride 50 mg/ kg) in wild-type C57BL6 mice (WT) and WT mice with myocyte-specific overexpression of NOS3 (TG), using a 13-MHz ultrasound probe (Sequoia, Acuson, Mountain View, CA). Invasive measurements of LV pressure and volume were obtained with a 1.4F pressure-volume catheter (SPR-839, Millar Instruments, Houston TX) (7 h after challenge with endotoxin or saline). At baseline, WT and TG mice had comparable measures of LV function. However, as assessed by echocardiography, the endotoxin-induced decrease in LV fractional shortening was attenuated in TG mice (from 54 ± 1 to 40 ± 1%) as compared to WT mice (from 56 ± 1 to 31 ± 2%). Invasive hemodynamics revealed that, compared to salinechallenged mice, dP/dtmax and cardiac output (CO) were markedly impaired in WT but not in TG 7 h after endotoxin challenge (Table 1).

The classic response to isolated endotoxin challenge entails secretion of IL-1 and TNFα . The purpose of this study was to longitudinally characterize the cytokine response to sepsis in critically ill systemic inflammatory response syndrome (SIRS) patients.

The lipid A antagonist E-5531 is the first agent that has been shown to block or ameliorate all the effects of bacterial lipopolysaccharide [LPS] endotoxin in a human endotoxin challenge model, according to study results presented at the 7th International IBC Conference on Sepsis [Washington DC, US; April 1997]. Treatment with E-5531 was one of 3 new methods of neutralising the effects of LPS in Gram-negative sepsis that were presented at the conference. The other approaches discussed were the use of the lipid A biosynthesis inhibitor L-573655 and its analogues, and the administration of reconstituted HDL-cholesterol for clearing LPS from the circulation. According to leading researchers in the field, blocking the effects of LPS may be the key to reducing mortality and morbidity rates in sepsis.